Rheumatoid Arthritis Gout | Arthritis or Gout
Systemic lupus erythematosus and gouty arthritis: an uncommon association. OBJECTIVE: To examine the frequency of gouty arthritis in patients with systemic . Q: I am a year-old man recently diagnosed with rheumatoid arthritis (RA). But I have had joint symptoms for some time, beginning two years ago with a bout of. Background Patients with systemic lupus erythematosus (SLE) often suffer from However, the association with gout – an independent cardiovascular risk.
Systemic lupus erythematosus and gouty arthritis: an uncommon association.
It sounds to me like you have gouty arthritis, or gout, an inflammatory disease that occurs when excess uric acid a bodily waste product circulating in the bloodstream is deposited as sodium urate crystals in certain joints. The excess uric acid may be caused by genetic factors or kidney disease. The condition may be aggravated by certain drugs such as diuretics and low doses of aspirin or by consuming too much alcohol or foods rich in purines, which are broken down into uric acid.
If your physician didn't know about your previous problems, it's not surprising he diagnosed your condition as rheumatoid arthritis; gout was probably not even on the radar. In its later stages gout can look a lot like RA, causing pain and inflammation in multiple joints. In some cases, untreated gout can be associated with a positive rheumatoid factor, an antibody often detected in the blood of people with rheumatoid arthritis.
Uric Acid Levels in SLE Patients Associated With PH in New Study
Even buildups of sodium urate can form lumps under the skin that resemble the nodules fairly common in RA. But that's where the similarity ends. The causes and treatments are entirely different. RA may begin acutely in many joints or start gradually in several joints causing damage and pain. Initially, the involved joints are the knuckles, middle joints of the fingers, wrists, and joints that attach the toes to the feet.
Uric Acid Levels in SLE Patients Associated With PH in New Study | Pulmonary Hypertension News
Gout, on the other hand, often starts as your problem did — with excruciating pain and swelling in the big toe — and often follows a trauma such as an illness or injury. Subsequent attacks may occur off and on in other joints — primarily those of the foot and knee — before becoming chronic. In its chronic stage, gout can affect many joints, including those of the hands. But this can take a few years to happen.
Unlike rheumatoid arthritis, gout is a well-understood and highly treatable disease. If MSU crystals require near normal levels of complement proteins to induce inflammation then the presence of decreased complement levels in patients with active SLE may pose a barrier to urate-induced inflammation. Additionally, the inflammatory response in acute gouty arthritis is in large part a result of the interaction between polymorphonuclear PMN cells and MSU crystals.
This interaction results in ingestion of MSU by PMN cells, and release of cytokines resulting in an intense inflammatory response. Granulocytes in SLE patients have been demonstrated to have impaired phagocytosis, which may be one of the reasons why patients with active SLE are unable to mount an adequate inflammatory response to MSU crystals [ 27 — 30 ].
Another potential explanation for the negative association between gout and lupus may be a change in structure of the MSU crystal in lupus patients because of a protein coat apo B lipoprotein that makes the crystal less inflammatory.
MSU crystals incubated with serum become less stimulatory for the leucocyte. This is mainly due to the binding of apo B lipoprotein to the MSU crystal [ 26 ]. Patients with SLE are frequently on corticosteroids. Glucocorticosteroid-associated lipid abnormalities include hypertriglyceridaemia, hypercholesterolaemia and a raised low-density lipoprotein LDL cholesterol level. The major apolipoprotein of LDL is apo B.
A high serum LDL level translates into a high serum apo B level, which has been shown to inhibit cellular responses to the MSU crystals by binding to the crystal surface, thereby physically inhibiting particle—cell interaction and subsequent phagocytosis of MSU and membrane activation.
Finally, it is important to remember that the mainstays of SLE treatment are corticosteroids, which are potent anti-inflammatory agents. Corticosteroids block increased vascular permeability associated with inflammation; they also suppress chemotaxis and phagocytosis by neutrophils. Treatment with corticosteroids, along with the other mechanisms for decreased MSU-mediated inflammation in lupus as outlined above, may explain why some lupus patients have been noted to have urate deposition in their skin and subcutaneous tissue but lack a history of acute arthritis.
Management of gout can be challenging in patients with SLE and renal insufficiency; levels of both colchicine and allopurinol have to be prescribed according to the patient's renal function. Corticosteroids can be used to manage acute gout flares. Non-steroidal anti-inflammatory drugs are not recommended.
Urate oxidase is being evaluated in some clinical trials for the treatment of gout, and if approved it may be useful in this clinical scenario. In summary, our review confirms that gouty arthritis is uncommon in SLE patients. It is typically observed in patients with long-standing SLE. Patients with a history of lupus nephritis and those on diuretics are at higher risk for developing gout.